No-Reflow Phenomenon and Endothelial Glycocalyx of Microcirculation

Maksimenko, A. V.; Турашев, А. Д.

doi:10.1155/2012/859231

Cited by 27 publications

(37 citation statements)

References 89 publications

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“…We surmise that an EGL which is depleted in sulfate content has elevated microvascular interfacial tension, a key risk factor for insulin resistance [283,285]. Cationic surfactants generally associate with GAGs, e.g., the EGL of the vascular system [249,250,[284][285][286][287][288], disabling their protection against water stress. The process of expelling cationic surfactants via the kidney necessarily further depletes the sulfate supply.…”

Section: Acute Shock and Role Of Endothelial Nos-derived No In Sdsmentioning

confidence: 96%

“…Shedding of the EGL during acute hyperglycemia has been shown to coincide with endothelial dysfunction, including increased permeability of the endothelium, increased reactive oxygen species (ROS), reduced nitric oxide (NO) synthesis, and coagulation activation in vivo [272]. It is entirely possible that the underlying, shared, pathophysiology is elevated microvascular interfacial tension [216,[284][285][286][287], as has been discussed previously. We surmise that an EGL which is depleted in sulfate content has elevated microvascular interfacial tension, a key risk factor for insulin resistance [283,285].…”

Section: Acute Shock and Role Of Endothelial Nos-derived No In Sdsmentioning

confidence: 99%

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The Initial Common Pathway of Inflammation, Disease, and Sudden Death

Davidson¹,

Seneff²

2012

Entropy

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Abstract:In reviewing the literature pertaining to interfacial water, colloidal stability, and cell membrane function, we are led to propose that a cascade of events that begins with acute exogenous surfactant-induced interfacial water stress can explain the etiology of sudden death syndrome (SDS), as well as many other diseases associated with modern times. A systemic lowering of serum zeta potential mediated by exogenous cationic surfactant administration is the common underlying pathophysiology. The cascade leads to subsequent inflammation, serum sickness, thrombohemorrhagic phenomena, colloidal instability, and ultimately even death. We propose that a sufficient precondition for sudden death is lowered bioavailability of certain endogenous sterol sulfates, sulfated glycolipids, and sulfated glycosaminoglycans, which are essential in maintaining biological equipose, energy metabolism, membrane function, and thermodynamic stability in living organisms. Our literature review provides the basis for the presentation of a novel hypothesis as to the origin of endogenous bio-sulfates which involves energy transduction from sunlight. Our hypothesis is amply supported by a growing body of data showing that parenteral administration of substances that lower serum zeta potential results in kosmotropic cationic and/or chaotropic anionic interfacial water stress, and the resulting cascade.Keywords: inflammation; serum sickness; colloidal instability; interfacial water stress; bio-sulfates; Shwartzman phenomena; sudden death syndrome Glossary of TermsAnaphylaxis a severe, rapidly progressing, life-threatening, generalized allergic reaction. Biological equipoise a stable, non-equilibrium, dissipative system synonymous with life. Cholesterol sulfate (Ch-S)quantitatively the most important known sterol sulfate in human plasma where it regulates the activity of the serine proteases, in cell membranes where it has a stabilizing role, and in platelet membranes where it supports platelet adhesion. Coherence domain (CD)a water CD is a collection of liquid water molecules which oscillate in unison in tune with a self-trapped electromagnetic field at a well-defined frequency. The coherent oscillations produce an ensemble of quasi-free electrons, able to collect noise energy from the environment and transform it into high-grade coherent energy in the form of electron vortices. This high-grade energy may then activate biomolecules resonating with the water CD. Colloidal instabilitya property attributed to a colloidal suspension that develops when stabilizing repulsive steric and electrostatic forces between colliding particles are insufficient to prevent their natural tendency to aggregate into masses large enough to precipitate.Colloidal suspension a colloid that has a continuous liquid phase in which a solid is suspended in a liquid, e.g., our flowing blood. Exclusion zone (EZ)a glass-like, gel phase consisting of water CDs resonating in-phase, adjacent to hydrophilic surfaces, several hundred micrometers wide which excludes colloi...

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Section: Acute Shock and Role Of Endothelial Nos-derived No In Sdsmentioning

confidence: 96%

Section: Acute Shock and Role Of Endothelial Nos-derived No In Sdsmentioning

confidence: 99%

The Initial Common Pathway of Inflammation, Disease, and Sudden Death

Davidson¹,

Seneff²

2012

Entropy

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“…47,[56][57][58] Reperfusion of the ischaemic myocardium is accompanied by a complex cascade of events, including endothelial swelling and destruction, platelet and neutro phil plugging, rouleaux formation of erythrocytes, and injury to the glycocalyx that lines the endothelium. [59][60][61][62] Reperfusion might, therefore, lead to mechanical destruction of the injured microvasculature. An early expression of endothelial distress and potential injury is the formation of endothelial blebs.…”

Section: The Role Of Ischaemiamentioning

confidence: 99%

Intramyocardial haemorrhage after acute myocardial infarction

et al. 2014

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In patients with acute myocardial infarction (AMI), the guideline-recommended treatment is mechanical revascularization by percutaneous coronary intervention (PCI), which is effective at reducing mortality. However, a substantial proportion of patients with AMI develop chronic cardiac failure owing to poor restoration of microvascular function and myocardial perfusion, despite restoration of epicardial vessel patency. This occurrence is called the 'no-reflow' phenomenon. Although pathological and clinical observations initially seemed to support the hypothesis that no-reflow was the result of microvascular obstruction, irreversible microvascular injury and subsequent intramyocardial haemorrhage are now also thought to be important factors in this process. Intramyocardial haemorrhage shares several pathophysiological features with the haemorrhagic transformation that occurs after ischaemic stroke. Understanding of the role of intramyocardial haemorrhage in the no-reflow phenomenon and myocardial injury is crucial to the development of new therapeutic strategies to treat AMI. In this Review, we provide a comprehensive overview of the pathogenesis and clinical relevance of intramyocardial haemorrhage, and discuss diagnostic options and future therapeutic strategies.

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“…Using such approach it is possible to determine involvement of both neutral saccharides and glycoca lyx degradation products in the development of vascu lar lesions [29]. The latter is important in the case of microcirculation lesions [30] and may be analyzed in vivo by means of HU and HU CS. …”

Section: Resultsmentioning

confidence: 99%

Do electrostatic interactions determine glycation of hyaluronidase derivatives with N-acetylhexosamines?

Турашев

Tischenko

Maksimenko

2012

Biochem. Moscow Suppl. Ser. B

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Using N acetylglucosamine and N acetylgalactosamine as model agents for glycation of native hyaluronidase and its chondroitin sulfate modified form it has been shown that the modified enzyme exhib ited higher inactivation than the native enzyme, while heparin caused similar inhibition of both forms. Such effect could be attributed to the development of electrostatic interactions as the modified hyaluronidase had altered surface electrostatic potential after chondroitin sulfate binding. However, variations in ionic strength of the medium containing enzyme derivatives have shown that their endoglycosidase activity changed in a similar manner and the effect on glycation represents a multifactor process. N acetylhexosamines are natural labels of endothelial glycocalyx degradation products. Interaction of the hyaluronidase forms with charged hyaluronan fragments revealed significantly higher inactivation of the modified enzyme compared with the native enzyme. The glycation pattern observed in this study was opposite to that observed with mono and di saccharides. Thus, it appears that the investigated hyaluronidase derivatives represent an informative enzy matic test in vivo for determination of the dominant type of glycation agents in blood circulation and their origin.

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No-Reflow Phenomenon and Endothelial Glycocalyx of Microcirculation

Cited by 27 publications

References 89 publications

The Initial Common Pathway of Inflammation, Disease, and Sudden Death

The Initial Common Pathway of Inflammation, Disease, and Sudden Death

Intramyocardial haemorrhage after acute myocardial infarction

Do electrostatic interactions determine glycation of hyaluronidase derivatives with N-acetylhexosamines?

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